| Project/Area Number |
24590120
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Takeshi 同志社女子大学, 薬学部, 教授 (80255380)
HORIGUCHI Kazuhide 福井大学, 医学部, 准教授 (20377451)
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| Co-Investigator(Renkei-kenkyūsha) |
MISAWA Hidemi 慶応大学, 薬学部, 教授 (80219617)
MORIWAKI Yasuhiro 慶応大学, 薬学部, 講師 (00392150)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | アセチルコリン / ニコチン受容体 / T細胞 / 樹状細胞 / Th0 / SLURP-1 / Th1 / alpha7 / Treg / α7 / α7ニコチン受容体 / CD205 / コリン・アセチルトランスフェレース / methyllycaconitine / α7 nAChR / アロステリック・リガンド / 扁桃 |
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| Outline of Final Research Achievements |
In the current project, we investigated the localization of SLURP-1, an endogenous allosteric ligand for alpha7 nAChRs, in immune organs and its role in regulation of T cell function together with effects of nicotine on T cell differentiation. Using immunohistochemical techniques, we found specific SLURP-1 localization in CD205-positive dendritic cells residing in the marginal zone of the human tonsil. SLURP-1 attenuated the growth of human leukemic T cell line MOLT-3 cells and human blood mononuclear cells (MNLs), but increased ACh synthesis in these cells, suggesting facilitation of functional development of T cells by SLURP-1. Nicotine suppressed differentiation of Th0 cells to Tregs, but facilitated to Th1 in mouse spleen MNLs, suggesting a role for nAChRs in T cell differentiation.
These results suggest that SLURP-1 plays a role in T cell development and differentiation during antigen presentation through stimulation of alpha7 nAChRs.
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